3-(Pyridin-4-ylmeth­oxy)phenol

In the title compound, C12H11NO2, the phenolic ring is inclined at an angle of 32.70 (1)° with respect to the pyridine ring. In the crystal, inter­molecular O—H⋯N hydrogen bonds link the mol­ecules into C(11) chains along [001]

catena-Poly[[[aqua­(pyridine-4-carboxyl­ato-κN)silver(I)]-μ-hexa­methyl­ene­tetra­amine-κ2 N:N′] dihydrate]

In the title compound, {[Ag(C6H4NO2)(C6H12N4)(H2O)]·2H2O}n, the AgI atom shows a distorted triangular pyramidal geometry,, formed by two N atoms from two hexa­methyl­ene­tetra­amine (hmt) ligands and one N atom from a pyridine-4-carboxyl­ate (4-pdc) ligand and one water mol­ecule. The hmt ligands bridge the Ag atoms, forming a chain along [001]. The carboxyl­ate group of the 4-pdc ligand is uncoordinated. O—H⋯O hydrogen bonds between the water mol­ecules and carboxyl­ate groups stabilize the structure

Bis[6-(1H-benzimidazol-2-yl-κN 3)pyridine-2-carboxyl­ato-κ2 N,O]cobalt(II) dihydrate

In the title compound, [Co(C13H8N3O2)2]·2H2O, the CoII atom has a distorted octa­hedral environment defined by four N atoms and two O atoms from two 6-(1H-benzimidazol-2-yl)pyridine-2-carboxyl­ate ligands. In the crystal, the complex mol­ecules and uncoordinated water mol­ecules are linked via N—H⋯O and O—H⋯O hydrogen bonds, forming a two-dimensional supra­molecular structure parallel to (010). π–π inter­actions are present between the imidazole, pyridine and benzene rings [centroid–centroid distances = 3.528 (2), 3.592 (2), 3.680 (2) and 3.732 (3) Å]

Silence of lncRNA UCA1 Represses the Growth and Tube Formation of Human Microvascular Endothelial Cells Through miR-195

Background/Aims: Recent studies have suggested that several lncRNAs contribute to the angiogenic function of endothelial cells. Herein, we set out to reveal whether lncRNA UCA1 has functions in endothelial angiogenesis. Methods: The expression levels of lncRNA UCA1, miR-195 and CCND1 in human microvascular endothelial HMEC-1 cells were altered by transfection. Subsequently, cell viability, migration, tube formation and apoptosis of HMEC-1 cells were respectively assessed. The cross-talk between lncRNA UCA1, miR-195, CCND1, and MEK/ERK and mTOR signaling pathways were investigated by performing qRT-PCR and Western blotting. Results: Silence of lncRNA UCA1 repressed HMEC-1 cells viability, migration, tube formation, and induced apoptosis. Meanwhile, silence of lncRNA UCA1 significantly up-regulated miR-195 expression. These alterations induced by lncRNA UCA1 were further enhanced by miR-195 overexpression, while were attenuated by miR-195 suppression. Moreover, silence of lncRNA UCA1 deactivated MEK/ERK and mTOR signaling pathways via a miR-195-dependent regulation. And the deactivation of MEK/ERK and mTOR signaling pathways led to a down-regulation of CCND1. Conclusion: This study demonstrates that silence of lncRNA UCA1 largely represses microvascular endothelial cells growth and tube formation. Silence of lncRNA UCA1 exerts its function possibly via up-regulation of miR-195, which in turn inactivates MEK/ERK and mTOR signaling pathways, and ultimately represses CCND1 expression

Poly[diaqua­bis­[μ-1-hy­droxy-2-(imidazol-3-ium-1-yl)ethane-1,1-diyldiphospho­nato]tricopper(II)]

In the title coordination polymer, [Cu3(C5H7N2O7P2)2(H2O)2]n, one CuII atom is five-coordinated by five O atoms from three 1-hy­droxy-2-(imidazol-3-ium-1-yl)ethane-1,1-diyldiphospho­nate (L) ligands in a distorted square-pyramidal geometry. The other CuII atom, lying on an inversion center, is six-coordinated in a distorted octa­hedral geometry by four O atoms from two L ligands and two O atoms from two water mol­ecules. The five-coordinated CuII atoms are linked by phospho­nate O atoms of the L ligands, forming a polymeric chain. These chains are further linked by the six-coordinated Cu atoms into a layer parallel to (01). N—H⋯O and O—H⋯O hydrogen bonds connect the layers into a three-dimensional supra­molecular structure

Identification of Prognostic Value of Rs3735590 Polymorphism in 3’-Untranslated Region (3’-UTR) of Paraoxonase 1 (PON-1) in Chronic Obstructive Pulmonary Disease Patients who Received Coronary Artery Bypass Grafting (CABG)

Background/Aims: In the treatment of serious and symptomatic coronary heart disease (CHD), coronary artery bypass grafting (CABG) is a frequently utilized intervention. In addition, the risk of CHD is strongly associated with the low activity of paraoxonase-1 (PON1), whose 3’-UTR harbors an rs3735590 polymorphism. The aim of this study was to investigate whether the rs3735590 polymorphism could be used as a prognosis marker in chronic obstructive pulmonary disease (COPD) patients undergoing CABG. In addition, the hypothesis, i.e., the rs3735590 polymorphism may be involved in the regulation of PON1 gene expression via modulating its interaction with miRNAs, was tested in this study. Methods: 292 patients diagnosed with COPD and treated with CABG were recruited for this study. Genomic DNA was extracted from clinical samples, and real-time quantitative PCR and Western-blot were used to measure the expression of miR-616 and PON1 in liver cells of different genotypes. Results: 292 COPD patients were divided into three groups according to their genotypes, i.e., rs3735590: CC (212), TC (75), and TT (5), respectively (TC and TT were merged in one group of T carriers for statistical analyses). Patients with the CC genotype were associated with a shorter event-free survival time as compared to patients with the T genotypes. In addition, PON1 was confirmed as a direct target gene of miR-616, while experiments with primary cells of different genotypes showed that miR-616 inhibited the expression of PON1 in CC cells. On the contrary, rs3735590 impaired such inhibitory effect of miR-616 in TT cells. Conclusion: The rs3735590 polymorphism of PON1 acts as a prognostic biomarker in COPD patients treated by CABG

ApoG2 induces cell cycle arrest of nasopharyngeal carcinoma cells by suppressing the c-Myc signaling pathway

<p>Abstract</p> <p>Background</p> <p>apogossypolone (ApoG2) is a novel derivate of gossypol. We previously have reported that ApoG2 is a promising compound that kills nasopharyngeal carcinoma (NPC) cells by inhibiting the antiapoptotic function of Bcl-2 proteins. However, some researchers demonstrate that the antiproliferative effect of gossypol on breast cancer cells is mediated by induction of cell cycle arrest. So this study was aimed to investigate the effect of ApoG2 on cell cycle proliferation in NPC cells.</p> <p>Results</p> <p>We found that ApoG2 significantly suppressed the expression of c-Myc in NPC cells and induced arrest at the DNA synthesis (S) phase in a large percentage of NPC cells. Immunoblot analysis showed that expression of c-Myc protein was significantly downregulated by ApoG2 and that the expression of c-Myc's downstream molecules cyclin D1 and cyclin E were inhibited whereas p21 was induced. To further identify the cause-effect relationship between the suppression of c-Myc signaling pathway and induction of cell cycle arrest, the expression of c-Myc was interfered by siRNA. The results of cell cycle analysis showed that the downregulation of c-Myc signaling pathway by siRNA interference could cause a significant arrest of NPC cell at S phase of the cell cycle. In CNE-2 xenografts, ApoG2 significantly downregulated the expression of c-Myc and suppressed tumor growth <it>in vivo</it>.</p> <p>Conclusion</p> <p>Our findings indicated that ApoG2 could potently disturb the proliferation of NPC cells by suppressing c-Myc signaling pathway. This data suggested that the inhibitory effect of ApoG2 on NPC cell cycle proliferation might contribute to its use in anticancer therapy.</p